MicroRNA miR ‐927 targets the juvenile hormone primary response gene Krüppel homolog1 to control Drosophila developmental growth

2020 ◽  
Vol 29 (6) ◽  
pp. 545-554
Author(s):  
Q. He ◽  
Y. Zhang ◽  
W. Dong
Keyword(s):  
Juvenile Hormone ◽  
Primary Response ◽  
Response Gene ◽  
Primary Response Gene ◽  
Developmental Growth

scholarly journals Structure and expression of TIS21, a primary response gene induced by growth factors and tumor promoters

1991 ◽  
Vol 266 (22) ◽  
pp. 14511-14518
Author(s):  
B.S. Fletcher ◽  
R.W. Lim ◽  
B.C. Varnum ◽  
D.A. Kujubu ◽  
R.A. Koski ◽  
...  
Keyword(s):  
Growth Factors ◽  
Primary Response ◽  
Tumor Promoters ◽  
Response Gene ◽  
Primary Response Gene

scholarly journals The novel primary response gene MyD118 and the proto-oncogenes myb, myc, and bcl-2 modulate transforming growth factor beta 1-induced apoptosis of myeloid leukemia cells.

1994 ◽  
Vol 14 (4) ◽  
pp. 2352-2360 ◽  
Author(s):  
M Selvakumaran ◽  
H K Lin ◽  
R T Sjin ◽  
J C Reed ◽  
D A Liebermann ◽  
...  
Keyword(s):  
Cell Death ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Growth Arrest ◽  
Primary Response ◽  
Tgf Beta ◽  
Response Gene ◽  
Primary Response Gene ◽  
Growth Factor Beta ◽  
Induced Apoptosis

Cell numbers are regulated by a balance among proliferation, growth arrest, and programmed cell death. A profound example of cell homeostasis, controlled throughout life, is the complex process of blood cell development, yet little is understood about the intracellular mechanisms that regulate blood cell growth arrest and programmed cell death. In this work, using transforming growth factor beta 1 (TGF beta 1)-treated M1 myeloid leukemia cells and genetically engineered M1 cell variants, the regulation of growth arrest and apoptosis was dissected. Blocking of early expression of MyD118, a novel differentiation primary response gene also shown to be a primary response gene induced by TGF beta 1, delayed TGF beta 1-induced apoptosis, demonstrating that MyD118 is a positive modulator of TGF beta 1-mediated cell death. Elevated expression of bcl-2 blocked the TGF beta 1-induced apoptotic pathway but not growth arrest induced by TGF beta 1. Deregulated expression of either c-myc or c-myb inhibited growth arrest and accelerated apoptosis, demonstrating for the first time that c-myb plays a role in regulating apoptosis. In all cases, the apoptotic response was correlated with the level of MyD118 expression. Taken together, these findings demonstrate that the primary response gene MyD118 and the c-myc, c-myb, and bcl-2 proto-oncogenes interact to modulate growth arrest and apoptosis of myeloid cells.

Myeloid differentiation primary response gene 88 (MyD88) deficiency in a large kindred

2010 ◽  
Vol 126 (1) ◽  
pp. 172-175 ◽  
Author(s):  
Daniel H. Conway ◽  
Jasmeen Dara ◽  
Asen Bagashev ◽  
Kathleen E. Sullivan
Keyword(s):  
Primary Response ◽  
Myeloid Differentiation ◽  
Response Gene ◽  
Primary Response Gene

scholarly journals Inhibition of Early Response Genes Prevents Changes in Global Joint Metabolomic Profiles in Mouse Post-Traumatic Osteoarthritis

2018 ◽  
Author(s):  
Dominik R. Haudenschild ◽  
Alyssa K. Carlson ◽  
Donald L. Zignego ◽  
Jasper H.N. Yik ◽  
Jonathan K. Hilmer ◽  
...  
Keyword(s):  
Transcriptional Activation ◽  
Cellular Responses ◽  
Early Response ◽  
Primary Response ◽  
Response Gene ◽  
Joint Injury ◽  
Non Invasive ◽  
Primary Response Gene ◽  
Post Traumatic ◽  
Early Response Genes

Osteoarthritis (OA) is the most common degenerative joint disease, and joint injury increases the risk of OA by 10-fold. Although the injury event itself damages joint tissues, a substantial amount of secondary damage is mediated by the cellular responses to the injury. Cellular responses include the production and activation of proteases (MMPs, ADAMTSs, Cathepsins), the production of inflammatory cytokines, and we hypothesize, changes to the joint metabolome. The trajectory of cellular responses is driven by the transcriptional activation of early response genes, which requires Cdk9-dependent RNA Polymerase II phosphorylation. Flavopiridol is a potent and selective inhibitor of Cdk9 kinase activity, which prevents the transcriptional activation of early response genes. To model post-traumatic osteoarthritis, we subjected mice to non-invasive ACL-rupture joint injury. Following injury, mice were treated with flavopiridol to inhibit Cdk9-dependent transcriptional activation, or vehicle control. Global joint metabolomics were analyzed 1 hour after injury. We found that injury induced metabolomic changes, including increases in Vitamin D3 metabolism and others. Importantly, we found that inhibition of primary response gene activation at the time of injury largely prevented the global changes in the metabolomics profiles. Cluster analysis of joint metabolomes identified groups of injury-induced and drug-responsive metabolites, which may offer novel targets for cell-mediated secondary joint damage. Metabolomic profiling provides an instantaneous snapshot of biochemical activity representing cellular responses, and these data demonstrate the potential for inhibition of early response genes to alter the trajectory of cell-mediated degenerative changes following joint injury.Significance StatementJoint injury is an excellent predictor of future osteoarthritis. It is increasingly apparent that the acute cellular responses to injury contribute to the initiation and pathogenesis of OA. Although changes to the joint transcriptome have been extensively studied in the context of joint injury, little is known about changes to small-molecule metabolites. Here we use a non-invasive ACL rupture model of joint injury in mice to identify injury-induced changes to the global metabolomic profiles. In one experimental group we prevented the activation of primary response gene transcription using the Cdk9 inhibitor flavopiridol. Through this comparison, we identified two sets of metabolites that change acutely after joint injury: those that require transcription of primary response genes, and those that do not.

scholarly journals Activation of the p21ras pathway couples antigen receptor stimulation to induction of the primary response gene egr-1 in B lymphocytes.

1995 ◽  
Vol 181 (1) ◽  
pp. 417-422 ◽  
Author(s):  
S B McMahon ◽  
J G Monroe
Keyword(s):  
B Lymphocytes ◽  
Cell Activation ◽  
Antigen Receptor ◽  
Primary Response ◽  
Dominant Negative ◽  
Mitogen Activated Protein Kinase ◽  
Cross Linking ◽  
B Cell Activation ◽  
Response Gene ◽  
Primary Response Gene

The primary response gene egr-1 encodes a sequence-specific transcription factor whose expression is necessary for antigen receptor-stimulated activation of B lymphocytes. The molecular processes involved in linking egr-1 induction to antigen receptor signaling have not been defined. The present study demonstrates that expression of an activated form of p21ras results in egr-1 induction similar to that previously shown after antigen receptor cross-linking. In addition, both antigen receptor cross-linking and p21ras use the same element in the egr-1 promoter to exert their effects. Using dominant-negative mutants of p21ras and raf-1, we demonstrate that induction of egr-1 after antigen receptor cross-linking is mediated by activation of the p21ras/mitogen-activated protein kinase signaling pathway. While regulation of the p21ras pathway during B cell activation has been intensively studied, this report represents the first description of a biologically relevant event associated with its activation.

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